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The sensation of pain (sensation of pain: 痛觉) cannot accurately be described as “located” at the point of an injury, or, for that matter (for that matter: so far as that is concerned), in any one place in the nerves or brain. Rather, pain signals—and pain relief—are delivered through a highly complex interacting circuitry. When a cell is injured, a rush of prostaglandins sensitizes nerve endings at the injury. Prostaglandins are chemicals produced in and released from virtually all mammalian cells when they are injured: these are the only pain signals that do not originate in the nervous system. Aspirin and other similar drugs (such as indomethacin and ibuprofen) keep prostaglandins from being made by interfering with an enzyme known as prostaglandin synthetase, or cyclooxygenase. The drugs’ effectiveness against pain is proportional to their success in blocking this enzyme at the site of injury. From nerve endings at the injury, pain signals move to nerves feeding into the spinal cord (spinal cord: n.脊髓). The long, tubular membranes of nerve cells carry electrical impulses. When electrical impulses get to the spinal cord, a pain-signaling chemical known as substance P is released there. Substance P then excites nearby neurons to send impulses to the brain. Local anesthetics such as novocaine and xylocaine work by blocking the electrical transmission along nerves in a particular area. They inhibit the flow of sodium ions through the membranes, making the nerves electrically quiescent; thus no pain signals are sent to the spinal cord or to the brain. Recent discoveries in the study of pain have involved the brain itself—the supervising organ that notices pain signals and that sends messages down to the spinal cord to regulate incoming pain traffic. Endorphins—the brain’s own morphine—are a class of small peptides that help to block pain signals within the brain itself. The presence of endorphins may also help to explain differences in response to pain signals, since individuals seem to differ in their ability to produce endorphins. It now appears that a number of techniques for blocking chronic pain—such as acupuncture and electrical stimulation of the central brain stem (brain stem: 脑干)—involve the release of endorphins in the brain and spinal cord.
这篇最后一道选错。。。对pain在nerve system 中的过程不是很清晰 4.It can be inferred from the passage that if the prostaglandin synthetase is only partially blocked, which of the following is likely to be true? (A) Some endorphins will be produced, and some pain signals will be intensified. (B) Some substance P is likely to be produced, so some pain signals will reach the brain. (C) Some sodium ions will be blocked, so some pain signals will not reach the brain. (D) Some prostaglandins will be produced, but production of substance P will be prevented.(B)
(E) Some peptides in the brain will receive pain signals and begin to regulate incoming pain traffic.
这个题是不是意思是 如果prostaglandin synthetase 只是部分的被抑制,那它的抑制作用就没有达到。。。pain还是可以继续传道? 问的有点白痴 但我的确不是很明白
想问一下这句When a cell is injured, a rush of prostaglandins sensitizes nerve endings at the injury. 是不是说当细胞被injured的时候, prostaglandins 使得细胞在injury结束的时候变得很敏感?
还有这句these are the only pain signals that do not originate in the nervous system. 是不是说疼痛信号prostaglandins 是产生于神经系统之外的。 结合后面的内容就是 pain signals产生于nerve system之外,然后From nerve endings at the injury(这句是不是说在injury结束的时候),pain signals进入神经细胞,然后随着神经细胞进入spinal cord,之后才有一系列的。。。
所以第4题 如果只是partially block the prostaglandin synthetase ,那就意味着对后面的process没有什么太大影响。。。
不知道这样理解对不对,希望大家指点我一下。。。 |
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